Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Temporal impact of sepsis on Alzheimer's disease pathology and neuroinflammation

ABSTRACT: Temporal impact of sepsis on Alzheimer's disease pathology and neuroinflammation

PROVIDER: PRJNA1237815 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Temporal impact of sepsis on Alzheimer's disease pathology and neuroinflammation

Project description:Epidemiological evidence has reported an associative link between sepsis survivorship and increased risk of dementia, particularly Alzheimer's disease (AD). Paradoxically, population studies show females are less susceptible to sepsis but more vulnerable to post-sepsis dementia, including Alzheimer's disease (AD). Here, we examined the temporal impacts of sepsis on AD pathology using an AD-model (TgCRND8) and wild-type mice, assessing outcomes at 7 days and 3 months post-sepsis. Following 7-days recovery, all male and female post-septic mice showed robust systemic immune activation. At this time, the female AD-model mice accumulated higher hippocampal amyloid-beta (Aβ) and upregulated AD-type transcriptomic signature. On the other hand, male AD-model mice showed no Aβ changes. Notably, wild-type post-septic males, but not females, displayed robust astrocytosis, with little change in microglial proliferation. By 3 months post-sepsis, microgliosis was specifically elevated in wild-type females, indicating a prolonged central immune response. At this time, both male and female AD-model mice showed exacerbated Aβ and anxiety. Gene network analysis revealed a stronger female immune response, while the male response was linked to estrogen receptor (ESR) signaling, with increased ERα protein observed in the brains of post-septic AD males. Together, our data highlights a sex-dimorphic temporal response in post-sepsis neuroinflammation, with ESR signaling playing a key role in males, while Aβ burden is affected similarly in both males and females.

2025-05-31 | GSE292277 | GEO

Temporal Cortex Alzheimer's Disease

Project description:Ion channel splice array data from temporal cortex brain tissue samples collected from Alzheimer's disease patients. Temporal cortex (Alzheimer's disease affected brain tissue structure) and cerebellum (Alzheimer's disease unaffected brain tissue structure) samples from control subjects were compared to temporal cortex and cerebellum of patients with Alzheimer's disease.

2010-06-11 | E-GEOD-6775 | biostudies-arrayexpress

Temporal lobe epilepsy and Alzheimer's disease

Project description:This SuperSeries is composed of the following subset Series: GSE6771: Temporal Cortex Control (mesial temporal lobe epilepsy control) GSE6773: Temporal neocortex mesial temporal lobe epilepsy GSE6774: Temporal Cortex Control (Alzheimer's disease control) GSE6775: Temporal Cortex Alzheimer's Disease GSE6777: Cerebellum Alzheimer's Disease GSE6778: Cerebellum Control (Alzheimer's disease control) Keywords: SuperSeries Refer to individual Series

2007-01-23 | E-GEOD-6834 | biostudies-arrayexpress

Temporal Cortex Control (Alzheimer's disease control)

Project description:Ion channel splice array data from temporal cortex brain tissue samples collected from control subjects (no Alzheimer's disease). Temporal cortex (Alzheimer's disease affected brain tissue structure) and cerebellum (Alzheimer's disease unaffected brain tissue structure) samples from control subjects were compared to temporal cortex and cerebellum of patients with Alzheimer's disease.

2010-06-11 | E-GEOD-6774 | biostudies-arrayexpress

Agilent 8x60K Custom Exon array of human temporal cortical tissue samples with varying degree of Alzheimer's Disease (AD)-related neurofibrillary pathology

Project description:In this study, we coupled microarray-based transcriptomics and MS-based phosphoproteomics assay to determine mRNA, protein, and phosphopeptide expression levels from 71 autopsied temporal cortical samples, with varying degree of Alzheimer's Disease (AD)-related neurofibrillary pathology. With computational analysis, we identified disease-related transcript, protein and phosphopeptide expression patterns, associated with distinct biological processes and cell types.

2018-12-16 | GSE106241 | GEO

Temporal Cortex Alzheimer's Disease

Project description:Ion channel splice array data from temporal cortex brain tissue samples collected from Alzheimer's disease patients. Keywords: disease associated splicing changes

2007-01-23 | GSE6775 | GEO

Temporal Cortex Control (Alzheimer's disease control)

Project description:Ion channel splice array data from temporal cortex brain tissue samples collected from control subjects (no Alzheimer's disease). Keywords: disease associated splicing changes

2007-01-23 | GSE6774 | GEO

GPR34 senses demyelination to promote neuroinflammation and cognition impairment in Alzheimer's disease

Project description:Sterile neuroinflammation initiated by damage-associated molecular patterns (DAMPs) has been regarded as an important driver in Alzheimer's disease (AD) and can occur prior or independently of the deposition of extracellular amyloid-β (Aβ) plaques and intracellular tau neurofibrillary tangles (NFTs). Genetic ablation or pharmacological inhibition of GPR34 reduced microglia activation, Aβ deposition and cognition impairment. Moreover, GPR34 inhibition prevented aging associated neuroinflammation and cognition impairment without the presence of Aβ plaques.

2025-02-05 | GSE216209 | GEO

Cerebellum Alzheimer's Disease

Project description:Ion channel splice array data from cerebellum brain tissue samples collected from Alzheimer's disease patients. Temporal cortex (Alzheimer's disease affected brain tissue structure) and cerebellum (Alzheimer's disease unaffected brain tissue structure) samples from control subjects were compared to temporal cortex and cerebellum of patients with Alzheimer's disease.

2010-06-11 | E-GEOD-6777 | biostudies-arrayexpress

Microbial infection instigates tau-related pathology in Alzheimer's disease via activating neuroimmune cGAS-STING pathway

Project description:Microbial infection, the strong trigger to directly induce inflammation in brain, is long considered a risk factor of Alzheimer's disease (AD), but how these infections contribute to neurodegeneration remains underexplored. To examine the effect of herpes simplex virus type 1 (HSV-1) infection on tauopathy in local hippocampus of P301S mice, we utilized a modified HSV-1 strain (mHSV-1) potentially relevant to AD, we found that its infection promotes tau-related pathology in part via activating neuroimmune cGAS-STING pathway in the tau mouse model. Specifically, Sting ablation causes the detectable improvement of neuronal dysfunction and loss in P301S mice, which is causally linked to lowered proinflammatory status in the brain. Administration of STING inhibitor H-151 alleviates neuroinflammation and tau-related pathology in P301S mice. These results jointly suggest that herpesviral infection, as the vital environmental risk factor, could induce tau-related pathology in AD pathogenesis partially via neuroinflammatory cGAS-STING pathway.

2024-04-11 | GSE229411 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data